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Commensal Enterococcus faecalis W5 ameliorates hyperuricemia and maintains the epithelial barrier in a hyperuricemia mouse model

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机构: [1]Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China [2]Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China [3]Department of Pathology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China [4]Department of Plastic Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, China
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关键词: Enterococcus faecalis epithelial barrier gastrointestinal microbiome hyperuricemia urate transporter

摘要:
Objective: The intestine is responsible for approximately one-third of uric acid (UA) excretion. The effect of commensal Enterococcus faecalis (E. faecalis), one of the most colonized bacteria in the gut, on UA excretion in the intestine remains to be investigated. The aim of this study was to evaluate the effect of commensal E. faecalis on UA metabolism and gut microbiota. Methods: The 16S rRNA gene sequencing was used to examine the species of Enterococcus in mouse fecal content. E. faecalis strain was isolated from mouse feces and identified to be E. faecalis W5. The hyperuricemia (HUA) animal model was established with yeast-rich forage and 250 mg & sdot;kg(-1)& sdot;day(-1) potassium oxonate. Oral administration of E. faecalis W5 was given for 20 days, serving as the Efa group. Results: Disrupted intestinal barrier, activated proinflammatory response and low UA excretion in the intestine were found in HUA mice. After E. faecalis W5 treatment, the gut barrier was restored and serum UA level was decreased. Additionally, fecal and intestinal UA levels were elevated, intestinal urate transporter ABCG2 and purine metabolism were upregulated. Moreover, short-chain fatty acid levels were increased, and intestinal inflammation was ameliorated. Conclusions: Commensal E. faecalis W5 ameliorated HUA through reversing the impaired gut barrier, promoting intestinal UA secretion by regulating ABCG2 expression, and decreasing intestinal UA synthesis by regulating purine metabolism. The results may provide the potential for developing treatments for HUA through the intestine.

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出版当年[2025]版:
最新[2023]版:
大类 | 3 区 医学
小类 | 4 区 胃肠肝病学
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Q3 GASTROENTEROLOGY & HEPATOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2024版] 出版当年五年平均 出版前一年[2023版]

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第一作者机构: [1]Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China
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通讯机构: [1]Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China [*1]Department of Gastroenterology, The Affiliated Hospital of Qingdao University, No. 16 Jiangsu Road, Qingdao, Shandong Province 266000, China
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